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代谢超重/肥胖表型与慢性心力衰竭患者死亡风险之间的关系。

Associations between metabolic overweight/obesity phenotypes and mortality risk among patients with chronic heart failure.

机构信息

School of Medicine, Nankai University, Tianjin, China.

The First Affiliated Hospital, Collage of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.

出版信息

Front Endocrinol (Lausanne). 2024 Sep 20;15:1445395. doi: 10.3389/fendo.2024.1445395. eCollection 2024.

DOI:10.3389/fendo.2024.1445395
PMID:39371927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11452845/
Abstract

BACKGROUND

Metabolic disorders and overweight or obesity are highly prevalent and intricately linked in patients with chronic heart failure (CHF). However, it remains unclear whether there is an interactive effect between these conditions and the prognosis of heart failure, and whether such an interaction is influenced by stratification based on age and sex.

METHODS

A total of 4,955 patients with CHF were enrolled in this study. Metabolic status was assessed according to the presence or absence of metabolic syndrome (MetS). BMI categories included normal weight and overweight or obesity (BMI < 24, ≥ 24 kg/m). Patients were divided into four phenotypes according to their metabolic status and BMI: metabolically healthy with normal weight (MHNW), metabolically unhealthy with normal weight (MUNW), metabolically healthy with overweight or obesity (MHO), and metabolically unhealthy with overweight or obesity (MUO). The incidence of primary outcomes, including all-cause and cardiovascular (CV) death, was recorded.

RESULTS

During a mean follow-up of 3.14 years, a total of 1,388 (28.0%) all-cause deaths and 815 (16.4%) CV deaths were documented. Compared to patients with the MHNW phenotype, those with the MUNW (adjusted hazard ratio [aHR], 1.66; 95% confidence interval [CI], 1.38-2.00) or MUO (aHR, 1.42 [95% CI, 1.24-1.63]) phenotypes had a greater risk of all-cause death, and those with the MHO phenotype (aHR, 0.61 [95% CI, 0.51-0.72]) had a lower risk of all-cause death. Moreover, the above phenomenon existed mainly among males and elderly females (aged ≥ 60 years). In nonelderly females (aged < 60 years), the detrimental effects of MetS were lower (aHR, 1.05 [95% CI, 0.63-1.75] among MUNW group and aHR, 0.52 [95% CI, 0.34-0.80] among MUO group), whereas the protective effects of having overweight or obesity persisted irrespective of metabolic status (aHR, 0.43 [95% CI, 0.26-0.69] among MHO group and aHR, 0.52 [95% CI, 0.34-0.80] among MUO group). Similar results were obtained in the Cox proportional risk analysis of the metabolic overweight/obesity phenotypes and CV death.

CONCLUSIONS

In male and elderly female patients with CHF, the detrimental effects of MetS outweighed the protective benefits of having overweight or obesity. Conversely, in nonelderly females, the protective effects of having overweight or obesity were significantly greater than the adverse impacts of MetS.

摘要

背景

代谢紊乱和超重或肥胖在慢性心力衰竭(CHF)患者中非常普遍且相互关联。然而,目前尚不清楚这些情况之间是否存在相互作用对心力衰竭预后的影响,以及这种相互作用是否受基于年龄和性别的分层的影响。

方法

本研究共纳入 4955 例 CHF 患者。根据代谢综合征(MetS)的有无来评估代谢状态。体重指数(BMI)类别包括正常体重和超重或肥胖(BMI<24、≥24kg/m²)。根据代谢状态和 BMI 将患者分为以下四组表型:代谢健康的正常体重(MHNW)、代谢不健康的正常体重(MUNW)、代谢健康的超重或肥胖(MHO)和代谢不健康的超重或肥胖(MUO)。记录主要结局(包括全因和心血管(CV)死亡)的发生率。

结果

在平均 3.14 年的随访期间,共记录到 1388 例(28.0%)全因死亡和 815 例(16.4%)CV 死亡。与 MHNW 表型患者相比,MUNW(调整后的危险比 [aHR],1.66;95%置信区间 [CI],1.38-2.00)或 MUO(aHR,1.42 [95% CI,1.24-1.63])表型患者的全因死亡风险更高,而 MHO 表型患者(aHR,0.61 [95% CI,0.51-0.72])的全因死亡风险较低。此外,这种现象主要存在于男性和老年女性(年龄≥60 岁)中。在非老年女性(年龄<60 岁)中,MetS 的有害影响较低(MUNW 组的 aHR 为 1.05[95% CI,0.63-1.75],MUO 组的 aHR 为 0.52[95% CI,0.34-0.80]),而超重或肥胖的保护作用仍然存在,无论代谢状态如何(MHO 组的 aHR 为 0.43[95% CI,0.26-0.69],MUO 组的 aHR 为 0.52[95% CI,0.34-0.80])。在对代谢性超重/肥胖表型与 CV 死亡的 Cox 比例风险分析中也得到了类似的结果。

结论

在男性和老年女性 CHF 患者中,MetS 的有害影响超过了超重或肥胖的保护作用。相反,在非老年女性中,超重或肥胖的保护作用明显大于 MetS 的不良影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/1ada57cae6f7/fendo-15-1445395-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/dab60640f6ee/fendo-15-1445395-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/1cab4711ca3b/fendo-15-1445395-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/24502c9e2d1c/fendo-15-1445395-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/1ada57cae6f7/fendo-15-1445395-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/dab60640f6ee/fendo-15-1445395-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/1cab4711ca3b/fendo-15-1445395-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/24502c9e2d1c/fendo-15-1445395-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b039/11452845/1ada57cae6f7/fendo-15-1445395-g004.jpg

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